{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T19:01:36Z","timestamp":1778612496475,"version":"3.51.4"},"reference-count":39,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2020,10,29]],"date-time":"2020-10-29T00:00:00Z","timestamp":1603929600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cell Biology International"],"published-print":{"date-parts":[[2021,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Dilated cardiomyopathy (DCM) is the leading cause of morbidity and mortality in diabetic patients. Long noncoding RNA plasmacytoma variant translocation 1 (PVT1) has been shown\u00a0to be related to the pathogenesis of DCM. However, the mechanism by which PVT1 regulates DCM pathogenesis is unclear. High glucose level was employed to construct a DCM cell model in vitro. Cell viability was determined via cell counting kit\u20108 assay. The level of lactate dehydrogenase (LDH) was measured with the\u00a0corresponding kit. Expression levels of PVT1, miR\u201023a\u20103p, and caspase\u201010 (CASP10) messenger RNA were evaluated with a quantitative real\u2010time polymerase chain reaction. Cell apoptosis was assessed by flow cytometry assay. Protein levels of B\u2010cell lymphoma 2\u2010associated X (Bax), cleaved\u2010caspase\u20103 (cleaved\u2010casp\u20103), and CASP10 were examined via western blot analysis. The relationship between PVT1 or CASP10 and miR\u201023a\u20103p was verified with dual\u2010luciferase reporter assay. We observed that PVT1 and CASP10 were upregulated while miR\u201023a\u20103p was downregulated in high glucose\u2010induced cardiomyocytes. High glucose levels repressed cardiomyocyte activity and induced cardiomyocyte apoptosis, but this influence was antagonized by PVT1 knockdown or miR\u201023a\u20103p overexpression. Furthermore, PVT1 acted as a sponge for miR\u201023a\u20103p, and miR\u201023a\u20103p inhibition counterbalanced the influence of PVT1 silencing on viability and apoptosis of cardiomyocytes under high glucose level treatment. PVT1 could increase CASP10 expression via sponging miR\u201023a\u20103p. In conclusion, PVT1 acted as a deleterious lncRNA in DCM. PVT1 facilitated cardiomyocyte death by regulating the miR\u201023a\u20103p\/CASP10, which offered a new mechanism to comprehend the pathogenesis of DCM.<\/jats:p>","DOI":"10.1002\/cbin.11479","type":"journal-article","created":{"date-parts":[[2020,10,13]],"date-time":"2020-10-13T19:28:31Z","timestamp":1602617311000},"page":"154-163","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Long noncoding RNA PVT1 facilitates high glucose\u2010induced cardiomyocyte death through the miR\u201023a\u20103p\/CASP10 axis"],"prefix":"10.1002","volume":"45","author":[{"given":"Yin\u2010Wen","family":"Xia","sequence":"first","affiliation":[{"name":"Department of Cardiology Hanchuan City People's Hospital  Hanchuan Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5603-3894","authenticated-orcid":false,"given":"Shao\u2010Bo","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Cardiology Hanchuan City People's Hospital  Hanchuan Hubei China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2020,10,29]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.00278.2006"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1385\/CT:3:3:219"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1186\/s10020-019-0074-5"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1177\/1753425919881778"},{"key":"e_1_2_8_6_1","first-page":"4471","article-title":"PVT1 regulates inflammation and cardiac function via the MAPK\/NF\u2010kappaB pathway in a sepsis model","volume":"16","author":"Feng F.","year":"2018","journal-title":"Experimental and Therapeutic Medicine"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.7150\/thno.31052"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.93.15.7464"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1209733"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-018-2760-9"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrcardio.2013.105"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng.3192"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrm1644"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1038\/srep36340"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0811371106"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1038\/s12276-019-0259-6"},{"key":"e_1_2_8_17_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.114.012285"},{"key":"e_1_2_8_18_1","doi-asserted-by":"publisher","DOI":"10.1002\/hep.30607"},{"key":"e_1_2_8_19_1","doi-asserted-by":"publisher","DOI":"10.14348\/molcells.2017.0012"},{"key":"e_1_2_8_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2017.08.034"},{"key":"e_1_2_8_21_1","doi-asserted-by":"publisher","DOI":"10.1002\/dmrr.3056"},{"key":"e_1_2_8_22_1","doi-asserted-by":"publisher","DOI":"10.7150\/thno.30516"},{"key":"e_1_2_8_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexmp.2013.11.005"},{"key":"e_1_2_8_24_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M414358200"},{"key":"e_1_2_8_25_1","doi-asserted-by":"publisher","DOI":"10.1186\/s12872-018-0939-5"},{"key":"e_1_2_8_26_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M406543200"},{"key":"e_1_2_8_27_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopha.2018.11.065"},{"key":"e_1_2_8_28_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCRESAHA.117.311802"},{"key":"e_1_2_8_29_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.diabres.2009.10.007"},{"key":"e_1_2_8_30_1","doi-asserted-by":"publisher","DOI":"10.1080\/1061186X.2017.1307379"},{"key":"e_1_2_8_31_1","first-page":"660","article-title":"miR\u201023a\u20103p suppresses cell proliferation in oral squamous cell carcinomas by targeting FGF2 and correlates with a better prognosis: miR\u201023a\u20103p inhibits OSCC growth by targeting FGF2","volume":"215","author":"Sun G.","year":"2019","journal-title":"Hepatology"},{"key":"e_1_2_8_32_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.241358198"},{"key":"e_1_2_8_33_1","doi-asserted-by":"publisher","DOI":"10.1038\/srep44265"},{"key":"e_1_2_8_34_1","doi-asserted-by":"publisher","DOI":"10.1158\/1078-0432.CCR-16-0742"},{"key":"e_1_2_8_35_1","first-page":"868","article-title":"PVT1\u2010derived miR\u20101207\u20105p promotes breast cancer cell growth by targeting STAT6","volume":"108","author":"Yan C.","year":"2017","journal-title":"Cancer Prevention Research"},{"key":"e_1_2_8_36_1","first-page":"5789","article-title":"The mechanism of miR\u201023a in regulating myocardial cell apoptosis through targeting FoxO3","volume":"21","author":"Yang Q. 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